An iatrogenic coronary arteriovenous fistula causing a steal phenomenon: an intracoronary Doppler study.

We present the case of a 67-year-old man in whom a guidewire broke at rotablation of the right coronary artery, creating an iatrogenic aneurysmal arteriovenous fistula to the coronary sinus. Successful Doppler wire-guided fistula occlusion by percutaneous coil embolization lead to normalization of coronary blood flow and relief of the patient's symptoms. Myocardial ischemia in this patient may have been due to a steal phenomenon caused by coronary artery fistulae, as suggested by blood flow velocity data obtained before and after fistula occlusion.

Directional coronary atherectomy: the Vienna experience.

BACKGROUND: Several multicenter trials have shown excellent results for directional coronary atherectomy (DCA) in a selected patient cohort. To prove the applicability of this method in daily clinical routine and a nonselected patient cohort, we analyzed 46 consecutive cases performed at our catheterization lab. METHODS: DCA was performed as a routine procedure in 45 suitable patients. Balloon dilatation or stent implantation postprocedure was accomplished only in case of unsatisfactory results. Quantitative coronary angiography was achieved pre- and postprocedure as well as at 6-month follow-up. RESULTS: Optimal atherectomy < 20% residual stenosis was reached in 24 (52%) of 46 target lesions and a residual stenosis < 50% in 46 (100%) lesions. Procedure-related complications occurred in three (6%) patients (one major complication, death, < 24 hours, 2%; two minor complications, pseudoaneurysm, 4%). The 6-month angiographic follow-up revealed a binary restenosis rate of 29% (n = 11). Ten out of 11 restenotic lesions required revascularization. When patients were stratified in two groups according to their preprocedural minimal lumen diameter (MLD), this parameter proved to be a very strong predictor of outcome. The percentage of restenosis was significantly higher in patients with an MLD > 1.60 mm compared to patients with a smaller MLD (54% vs 19.3%; P < 0.0001). Reference vessel diameter preprocedure did not differ significantly. CONCLUSIONS: Our study demonstrated that DCA is a suitable technique for the daily clinical routine, as the rates of complications and restenosis were similar to that in a highly selective patient cohort. Additionally, our study showed that patient selection should include preprocedural analysis of MLD in order to achieve optimal results. Therefore, atherectomy yielded comparable results to other conventional techniques and may be used instead of or in combination with them.

Heart rate variability in isolated rabbit hearts.

The presence of heart rate variability (HRV) in patients with cardiac denervation after heart transplantation raised our interest in HRV of isolated, denervated hearts. Hearts from seven adult white ELCO rabbits were transferred to a perfusion apparatus. All hearts were perfused in the working mode and in the Langendorff mode for 20 minutes each. HRV was analyzed in the frequency domain. A computer simulated test ECG at a constant rate of 2 Hz was used for error estimation of the system. In the isolated, denervated heart, HRV was of random, broadband fluctuations, different from the well-characterized oscillations at specific frequencies in intact animals. Mean NN was 423 +/- 51 ms in the Langendorff mode, 406 +/- 33 ms in the working heart mode, and 500 ms in the test ECG. Total power was 663 +/- 207 ms2, 817 +/- 318 ms2, and 3.7 ms2, respectively. There was no significant difference in any measure of HRV between Langendorff and working heart modes. The data provide evidence for the presence of HRV in isolated, denervated rabbit hearts. Left atrial and ventricular filling, i.e., the working heart mode, did not alter HRV, indicating that left atrial or ventricular stretch did not influence the sinus nodal discharge rate.

Management of acute myocardial infarction: evaluating the past, practicing in the present, elaborating the future.

The management of acute myocardial infarction initially focused on treatment and/or prevention of complications. In the prethrombolytic era, therapeutic regimens mainly comprised the use of antianginal and antiarrhythmic drugs. The development of semi-invasive hemodynamically guided treatment concepts led to remarkable improvement in clinical outcome. After the introduction of the "wave-front phenomenon," multiple pharmacologic treatment strategies were developed with the goal of infarct size reduction. The use of thrombolytic agents reduced infarct size and improved prognosis of patients with acute myocardial infarction. Acute angioplastic intervention was introduced in specialized centers to achieve rapid restoration of coronary blood flow. The protection of the myocardium from reperfusion injury, however, remains an unresolved issue. Intravenous magnesium administration in conjunction with new and better recanalization techniques could therefore be a promising therapy strategy in patients with acute myocardial infarction.

Acute myocardial infarction, reperfusion injury, and intravenous magnesium therapy: basic concepts and clinical implications.

The concept of reperfusion-induced injury has aroused special interest during the past decade as thrombolysis and direct angioplasty were introduced for early restoration of coronary blood flow in patients with acute myocardial infarction. There is experimental and clinical evidence that oxygen-derived free radicals (oxyradical hypothesis), activation of the complement system (complement hypothesis), and disturbance in calcium homeostasis (calcium hypothesis), may account for the development of reperfusion injury. Data from numerous animal experiments and clinical trials suggest that magnesium, a physiologic calcium blocker, may be efficacious for reduction of reperfusion injury. Despite encouraging results from previous clinical trials that revealed beneficial effects of intravenous magnesium therapy with respect to mortality, left ventricular function, and infarct size, a recently published large-scale trial (ISIS-4) provided conflicting data and caused major controversy. Further clinical trials, well-designed and carefully conducted, should elucidate the beneficial effects of magnesium in acute myocardial infarction, especially in conjunction with new and aggressive reperfusion techniques.

Cardiac depolarization and repolarization in Wolff-Parkinson-White syndrome.

Delta wave and QRS complex polarities have been extensively studied in preexcitation syndromes. However, only limited data exist about ventricular depolarization and repolarization in the setting of maximal preexcitation in relation to the site of insertion of the accessory pathway. Therefore this study was designed to systematically analyze cardiac depolarization and repolarization in patients with maximal preexcitation. We analyzed the polarity of the QRS complex and T wave on the frontal plane on the conventional 12-lead electrocardiogram in 118 patients with maximal preexcitation. Fast atrial pacing was used to provoke maximal ventricular preexcitation. The 32 patients with a left lateral accessory pathway showed right-axis deviation of the QRS complex (110 +/- 20 degrees) with a left-axis deviation of the T-wave axis (-40 +/- 25 degrees). The 54 patients with a posteroseptal accessory pathway had a left axis of the QRS complex (-50 +/- 20 degrees) with a right-axis deviation of the T-wave axis (95 +/- 15 degrees). The 11 patients with a right lateral accessory pathway had a left axis of the QRS complex (-40 +/- 20 degrees) and a right axis of the T wave (110 +/- 10 degrees). In 7 patients with a left anterolateral accessory pathway and 14 patients with a right anteroseptal accessory pathway, the axis of the QRS complex was 50 +/- 25 degrees and 45 +/- 20 degrees, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

The differential diagnosis on the electrocardiogram between ventricular tachycardia and preexcited tachycardia.

The 12-lead surface electrocardiogram is a simple and useful tool for the differential diagnosis of regular wide QRS complex tachycardia. However, criteria do not as yet exist to discriminate between ventricular tachycardia and supraventricular tachycardia with anterograde conduction over an accessory pathway (preexcited tachycardia). Therefore, we designed a new stepwise approach with three criteria for the electrocardiographic differential diagnosis between ventricular tachycardia and preexcited tachycardia and prospectively studied 267 regular tachycardias with electrophysiologically proven mechanism and a wide QRS complex (> or = 0.12 s): 149 consecutive ventricular tachycardias and 118 consecutive preexcited regular tachycardias. Underlying heart disease was old myocardial infarction in 133 of 149 (89%) ventricular tachycardias. The patients presenting with preexcited tachycardia had no additional structural heart disease. Atrial fibrillation with preexcited QRS complex was not included. The criteria favoring ventricular tachycardia were: (1) presence of predominantly negative QRS complexes in the precordial leads V4 to V6, (2) presence of a QR complex in one or more of the precordial leads V2 to V6, and (3) AV relation different from 1:1 (more QRS complexes than P waves). The final sensitivity and specificity of these three consecutive steps to diagnose ventricular tachycardia were 0.75 and 1.00, respectively. This new stepwise approach is sensitive and highly specific for the differential diagnosis between ventricular tachycardia in coronary artery disease and preexcited regular tachycardia.

Bedside recordings of His-bundle electrograms using conventional twelve-lead surface electrocardiography.

INTRODUCTION: Endocavitary His-bundle electrograms are usually recorded using high fidelity amplifiers and special filters. METHODS AND RESULTS: To evaluate whether similar recordings could be obtained using a 12-lead surface electrocardiograph, we compared recordings obtained during an electrophysiologic study in 33 patients to those obtained by connecting the two poles of the bipolar catheter, used during the study as the His catheter, to the right and left arm leads of the surface electrocardiograph. We recorded His-bundle electrograms using both techniques in all patients. There were no differences in measurements obtained between the two techniques. CONCLUSION: His-bundle electrograms can be recorded reliably with a conventional electrogram without sophisticated systems.

Right-sided versus left-sided radiofrequency ablation of the His bundle.

UNLABELLED: Radiofrequency (RF) ablation of the His bundle was attempted in 30 consecutive patients with atrial flutter or fibrillation. A 7 French quadripolar catheter with a 4-mm distal electrode was advanced from the right femoral vein (21 patients), or subclavian vein (two patients) and positioned across the tricuspid valve. Adequate His-bundle potentials were obtained in all patients. However, in six patients atrioventricular (AV) block could not be obtained after multiple (mean = 8) applications of RF energy from the conventional right-sided approach. In these patients the same catheter was advanced to record a His potential through a retrograde arterial approach. AV block was created in all patients with one to three applications of RF energy. The duration of the procedure was 22 to 90 minutes for the right-sided approach and 5 to 10 for the left-sided approach (P < 0.005). Subsequently, in seven patients a left-sided approach was used first. One to six applications of RF energy were required to create AV block. The radiation exposure time was 3 to 20 minutes. No complications occurred. CONCLUSIONS: RF ablation of the His bundle seems easier using a left-sided than a right-sided approach, reduces procedure and radiation time, and avoids recovery of conduction. These data suggest that a left-sided approach, in spite of requiring arterial catheterization, may be preferable to a right-sided approach.

Antiadrenergic cardiovascular adverse effects of high-dose amiodarone loading regimen.

A 55-year-old patient with inferior wall infarction was treated effectively for ventricular tachycardia with high-dose oral amiodarone loading regimen (5 g within 16 hours). Serial pharmacokinetic studies demonstrated a rapid temporary increase in amiodarone plasma concentration to a maximum of 3.40 micrograms/ml 17 hours after initiation of therapy followed by a return to normal plasma concentration within 8 hours. During fast drug evasion the patient developed acute low-output syndrome with syncope successfully controlled with intravenous catecholamine administration. Our findings suggest that the cardiovascular collapse was caused by the non-competitive adrenoceptor antagonism of amiodarone resulting in secondary autonomic insufficiency.

Radiofrequency ablation of symptomatic but benign ventricular arrhythmias.

Two cases are presented where ablation of severely symptomatic ventricular arrhythmias not responding to medical therapy was accomplished with radiofrequency current application. After a routine programmed stimulation protocol, a quadripolar ablation catheter with a 4-mm tip was advanced percutaneously into the left ventricle in one case and into the right ventricle in the second case; and after precise pace mapping, the arrhythmogenic focus was successfully ablated using radiofrequency current. The postablation ambulatory recording revealed virtual eradication of ventricular ectopy in both cases. In conclusion, in severely symptomatic cases of "benign" ventricular arrhythmias, radiofrequency ablation offers an effective therapeutic alternative.

Plasma propafenone concentration in the evaluation of anti-arrhythmic efficacy.

The anti-arrhythmic drug efficacy of oral propafenone therapy (300 mg to 900 mg per day) was studied in relation to propafenone and hydroxy-propafenone plasma concentrations in 70 outpatients (46 males, 24 females, mean age 57 +/- 12 years) followed up for 24 +/- 32 months. On average 1.7 plasma concentration measurements were performed per patient. The arrhythmias were effectively controlled in 32 patients, but in another 32 patients propafenone therapy was ineffective; in six patients the evaluation was unclear. The therapy was effective in 66% of patients with ventricular premature beats, in 50% with complex ventricular arrhythmias, in 40% with ventricular tachycardia and in 20% with supraventricular tachycardia. Fifty per cent of patients with coronary heart disease and electrical disease, but only 20% with dilated cardiomyopathy and Wolff-Parkinson-White syndrome were effectively treated. Measurement of peak plasma propafenone levels performed 4.5 +/- 2 h after oral drug administration revealed no statistically significant dose-plasma concentration relation. Optimal propafenone drug efficacy was documented at propafenone plasma concentrations ranging from 0.20 to 0.60 micrograms/ml (63% of patients considered as effectively treated). There was a trend to decrease propafenone efficacy at plasma concentrations below 0.20 micrograms/ml and above 0.60 micrograms/ml. Analysis of hydroxypropafenone identified four patients as poor metabolizers with unusually high propafenone and low hydroxypropafenone plasma concentrations; only one of these four patients showed drug efficacy. Monitoring of propafenone and hydroxypropafenone plasma concentrations was a practical procedure to assess patient's compliance, to identify poor metabolizers and to guide anti-arrhythmic drug therapy.

Successful therapy of the prostaglandin defect "Wien-Hietzing" (lack of platelet high-affinity binding sites for prostaglandin I2).

Some years ago we detected a lack of platelet high-affinity PGI2 binding sites in a 10 year-old girl who presented to the outpatient unit with clinical symptoms and signs of acute popliteal artery occlusion. We named this new defect in the prostaglandin system "Wien-Hietzing". Acute surgery was successful. On the basis of earlier findings that aspirin is able to sensitize platelets to the action of PGI2 and produce beneficial changes in platelet sensitivity, we decided to treat this girl with a daily dosage of 20 mg aspirin orally. Repeated control examinations during the total follow-up period of about 6 years revealed normalized platelet sensitivity and normalized receptor behaviour. The girl is symptom-free to date. It is concluded that this prostaglandin defect may be successfully treated with long-term, low-dose aspirin administration.

Effects of Hydergine on platelet deposition on "active" human carotid artery lesions and platelet function.

Effects of co-dergocrine mesylate (Hydergine), a drug widely used for the therapy of cerebral vascular disease on local platelet accumulation in the carotid artery region was studied by means of the platelet uptake ratio (PUR) and on the systemic platelet-vascular wall interaction as calculated from platelet half-life were investigated. A placebo controlled, double blind, randomised protocol was used, 18 patients were treated with co-dergocrine and compared to placebo (n = 18). Co-dergocrine treatment resulted in a significant decrease in platelet deposition, PUR decreased from 1.28 +/- 0.05 before treatment to 1.25 +/- 0.06 on day 5 of therapy with a statistically significant (p less than 0.001) in the paired comparison. In the control group the corresponding changes from 1.29 +/- 0.04 before to 1.28 +/- 0.04 did not show a p-value of less than 0.05 in paired comparison. Platelet half-life (72 +/- 11 before vs. 76 +/- 11 hours after 5 days of co-dergocrine treatment) showed a statistically significant (p less than 0.001) prolongation, whereas in the placebo group no relevant change of T/2 was observed (71 +/- 10 before vs. 72 +/- 10 hours on day 5, p greater than 0.10). No relevant effects on ADP-induced platelet aggregation, platelet-release reaction, platelet aggregate ratio, TXB2 plasma levels and thrombin-induced MDA-formation could be detected. These results indicate that co-dergocrine decreased in-vivo platelet residence time to atherosclerotic lesions of the carotid artery. Co-dergocrine may thereby be of benefit in prevention of mural thrombus formation and prevention of transient ischemic attacks, but also of atherosclerosis in man.

Early-onset thrombocytopenia during combination chemotherapy in testicular cancer is induced by vinblastine.

Platelet kinetics were studied in 70 patients with testicular cancer to elicit the agent responsible for chemotherapy-induced transient early-onset thrombocytopenia; 204 treatment courses were analyzed using three different therapy protocols, which contained vinblastine and bleomycin either alone or in combination with cisplatin. Platelet count decreased significantly from the start of vinblastine administration reaching its nadir on the third day of therapy in each of the three treatment groups. Between day 4 and day 10 of the treatment cycle, platelet counts steadily increased even in patients still receiving continuous bleomycin infusions. The conclusion that the observed early-onset thrombocytopenia was caused by vinblastine was substantiated by the outcome of two additional examinations. Platelet half-life was significantly shortened 24 hours after vinblastine administration and electron microscopy revealed a dissolution of cytoplasmatic microtubules with loss of the typical discoid shape of platelets within 15 minutes after the start of therapy. Both findings occurred irrespective of the specific treatment protocol, i.e., even after nothing but vinblastine had been given. These results strongly suggest that vinblastine is the main cytostatic agent responsible for the transient early-onset thrombocytopenia observed during chemotherapy of testicular cancer.

Recurrent paradoxical embolism complicating severe thromboembolic pulmonary hypertension.

A patient with a three-year history of recurrent pulmonary embolism is presented. Thromboembolic pulmonary hypertension was proven in the final stage of disease in the presence of repeated episodes of systemic embolic events. Paradoxical embolism was assumed to be present on the basis of blood-gas analysis and contrast echocardiography that demonstrated a right-to-left shunt at atrial level. Autopsy revealed a patent foramen ovale and provided strong evidence for the accuracy of the clinical diagnosis.

The platelet rebound phenomenon during PGI2-infusion occurs at the receptor level.

In 6 patients treated with continuous prostaglandin I2 (PGI2)-infusion using a portable pump at a rate of 5 ng/kg/min for 7 days drug receptor interaction of [3H]Iloprost, a stable PGI2 analogue, with a particulate platelet membrane fraction was investigated. Saturation binding experiments of the high affinity platelet prostacyclin receptor performed before and at the end of PGI2 infusion revealed a significant increase of dissociation constant (Kd) and increase in maximal number of binding sites (Bmax). These findings suggest that continuous long-term PGI2 infusion results in a functional desensitization of the membrane-bound PGI2 platelet receptor with a decrease in receptor affinity and an increase in number of binding sites as suggested earlier based upon platelet sensitivity behaviour.